Session 10 Flashcards

(80 cards)

1
Q

What is heart failure?

A

The inability of the heart to meet the demands of the body; a clinical syndrome (collection of signs) of reduced cardiac output, tissue hypoperfusion, increased pulmonary pressures and tissue congestion.

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2
Q

What enables the heart to function effectively?

A
  • One-way valves
  • Functioning cardiac muscle
  • Chamber size

Any impairment = impairment in cardiac function

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3
Q

What is the most common cause of heart failure?

A

Ischaemic heart disease that causes myocardial dysfunction through fibrosis and remodelling which impairs contractility of heart

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4
Q

What are the other causes of heart failure?

A
  • Hypertension (afterload)
  • Aortic stenosis (afterload)
  • Cardiomyopathies (dilation)
  • Arrhythmias
  • Pericardial disease
  • Acquired/congenital valvular or myocardial structures
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5
Q

What can cause high output heart failure and why?

A

Occurs when there is a very elevated demand on cardiac output (eg. during thyrotoxicosis) even for a healthy heart

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6
Q

How do you measure the cardiac output?

A

CO = SV x HR

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7
Q

What is stroke volume?

A

A fraction of the total volume within the ventricle at the end of diastole (EDV)

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8
Q

What is ejection fraction?

A

Stroke volume / EDV x 100

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9
Q

What can DECREASE stroke volume?

A

Total peripheral resistance (afterload) = More constriction in smooth muscle vessels means that less blood can get through

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10
Q

What can INCREASE stroke volume?

A
  • Pre load (increasing volume in ventricles at end of diastole as there is more stretch and a higher pressure)
  • Myocardial contractility
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11
Q

What is the Frank-Starling’s law?*

A

More ventricular distention during diastole will result in a greater volume of blood being ejected during systole (up to a certain point)

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12
Q

What can increase the contractility of the heart?*

A

Increased sympathetic activity (inotropy)

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13
Q

Why can cardiac output be reduced in heart failure?

A

Due to a reduction in stroke volume, which can be caused by:

  • Reduced preload (impaired ventricular filling)
  • Reduced myocardial contractility (unable to produce the force of contraction for given volume)
  • Increased afterload (higher pressure against which ventricles must contract)
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14
Q

What is DIASTOLIC heart failure?*

A
  • Problems with FILLING of the heart

- Reduced ventricular capacity (reduced space available in ventricle)

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15
Q

What can cause diastolic heart failure?

A
  • Ventricle muscle wall being hypertrophied
  • Ventricular chambers being too stiff and not relaxing enough
  • Ventricular muscle remodelling which has encroached the ventricular chamber size
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16
Q

Why is there a limit to which cardiac muscle can stretch?

A

Degree of overlap between actin and myosin = stretching too far means that they are pulled too far away from each other to effectively contract

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17
Q

What is SYSTOLIC heart failure?*

A
  • Space in heart available but there is a poor degree of ventricular contraction
  • Heart unable to empty as well because it can’t pump with enough force
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18
Q

What can cause systolic heart failure?

A
  • Thin or fibrosed muscle wall
  • Enlarged chambers due to overstretched sarcomeres
  • Abnormal/uncoordinated contraction
  • EJECTION PROBLEM
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19
Q

What is heart failure with reduced ejection fraction?*

HFrEF

A

Heart failure that causes systolic dysfunction (i.e. contractility problem)

Most common

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20
Q

What is heart failure with preserved ejection fraction?*

HFpEF

A

Heart failure that causes diastolic dysfunction and indicates a filling problem

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21
Q

What should the NORMAL ejection fracture?

A

Above 50% (normal usually above 60%)

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22
Q

What is REDUCED ejection fracture?

A

Below 40%

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23
Q

How can the heart be failing with a preserved ejection fraction?

A
  • The ventricle will eject less volume in a heart beat as it can only accommodate a smaller volume
    Fraction of what’s available is still above 50%, even though not all is ejected
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24
Q

How can you calculate the ejection fracture?

A

Echocardiogram (cheap, non-invasive)

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25
Which ventricle is most commonly involved in heart failure?
Left ventricle, but the right ventricle will be involved subsequently
26
What is congestive/biventricular heart failure?
Both ventricles being involved in heart failure
27
When can right ventricular heart failure occur in isolation and why?
Can occur secondary to chronic lung diseases due to changes in the pulmonary oxygenation of blood etc.
28
What is the most common cause for RV heart failure?
LV heart failure
29
What does an increase in LV filling in the healthy heart lead to?
A bigger increase in cardiac output
30
What does an increased LV filling cause in a failing heart?*
- Very small increase in CO - Worsening CO - Marked increase in LVEDP to increase SV, which can result in a failing CO and pulmonary congestion due to the pressure being so high that it impedes return of the blood from the lungs
31
What physiological mechanisms are triggered by drops in cardiac output that will correct it?*
- Damaged ventricular tissue - Reduction in efficiency of contraction - Reduced SV and therefore CO - NEURO-HORMONAL ACTIVATION
32
What can neuro-hormonal activation eventually cause?
Increased cardiac demand, which will reduce the stroke volume even more (helpful if the heart is healthy)
33
What is activated if cardiac output is reduced and BP drops?*
- Baroreceptors in carotid sinus and aortic arch detect BP drop - Increased sympathetic drive increases HR and TPR (so needing more oxygen) - Increased afterload and cardiac workload
34
How can the RAAS be activated?
- Drop in BP causes a drop in renal perfusion | - Activation of RAAS
35
What does RAAS do?*
- Increases circulating volume (Na+ and H20 retention) - ADH stimulated - Vasoconstriction - Enhanced sympathetic activity - Increased preload (which increases stretch more and WILL NOT HELP)
36
What can long-term activation of SNS and angiotensin II cause?
Cardiotoxic effects
37
What are the most common symptoms and signs of heart failure?
- Fatigue and lethargy (not perfused) - Breathlessness (depends on if RV or LV affected) - Leg swelling (oedema, pulmonary or peripheral)
38
How does tissue fluid form?* SLIDE 23!
High pressure in arterial circulation: H >> O (H out, O in = fluid into interstitium) Low pressure: O >> H (fluid back into capillary)
39
What causes tissue oedema?
Increased capillary hydrostatic pressure leading to less fluid being drawn back into venules (higher pressure = higher hydrostatic pressure)
40
What is pulmonary oedema?*
Accumulation of fluid in the lungs
41
What is peripheral oedema?*
Accumulation of fluid in the peripheries
42
What are the features of left ventricular heart failure? | *- caused by pulmonary oedema
Fluid in lungs - Fatigue and lethargy - Exertional breathlessness - Orthopnoea (breathlessness made worse lying flat)* - Paroxysmal nocturnal dyspnoea (waking up gasping for breath)* - Basal pulmonary crackles* - Cardiomegaly
43
What are the features of right ventricular heart failure?
Fluid in body - Fatigue and lethargy - Breathlessness - Peripheral/pitting oedema (tissue fluid accumulation) - Raised JVP - Liver congestion (smooth, tender, enlarged liver)
44
What is a raised jugular venous pressure used to diagnose and how is it relevant?*
- If distended = elevated - Is a marker of pressure in the right side of the heart - Will only go up if right side of heart is struggling
45
What is the risk of readmission/death within 60 days in heart failure?*
30-50%
46
What is the 'organ system failure' trajectory?*
- Patient constantly gradually declines - Has dips where they become acutely unwell - You never know if the patient will get better or if they will die - Death often 'sudden' but time is about 2-5 years from when they have to be hospitalised
47
What is Class I heart failure?
No symptomatic limitation of physical activity
48
What is Class II heart failure?
- Slight limitation of physical activity - Ordinary physical activity resulting in symptoms - No symptoms at rest
49
What is Class III heart failure?
- Marked limitation of physical activity - Less than ordinary physical activity = symptoms - No symptoms at rest
50
What is Class IV heart failure?
- Inability to carry out any physical activities without symptoms - Symptoms at rest - Discomfort increasing with any physical activity
51
What are the key questions to ask in investigations?
Does the patient have heart failure? - Diagnose with clinical investigations (symptoms, tests, etc) - Differential diagnoses? (eg. anaemia)
52
What is the next question?
What sort of heart failure does a patient have? - HFrEF - LV systolic dysfunction - Valvular/structural - RV failure - High output cardiac failure - HFpEF (stiffness)
53
What is the final question to ask?
What is causing the patient's heart failure? - Viral - Ischaemic heart disease - Hypertension
54
What is used to symptomatically treat heart failure?
Furosemide (diuretic to reduce fluid buildup)
55
What is the prognostic treatment for left ventricular systolic dysfunction?
- Cardiac rehabilitation - ACE/ARB (angiotensin receptor blockers) - Betablockers - MRA (Spironolactone) - aldosterone receptor antagonist - Biventricular pacemaker - Sacubitril valsartan - Ivabradine, nitrate, IV iron
56
What is the immediate treatment for an emergency heart failure?
- Furosemide (80mg stat) - Oxygen if hypoxic - Respiratory support?
57
What can cause tachycardia in heart failure ?
Pulmonary oedema (must be treated immediately!)
58
What can cause fast atrial fibrillation?*
Heart trying to decompensate
59
How does respiratory/heart failure present on a CXR?*
- Cardiomegaly - Fluid in fissure - Pleural effusion
60
Why is IV furosemide used?
- Reduces preload and therefore afterload - Immediate venodilation - Diuretic action 30 minutes, peak at 60-90 min - Getting rid of excess fluid AROUND 40mg NEEDED TO MAXIMISE DIURESIS IF KIDNEYS GOOD
61
What needs to be monitored when giving furosemide?
- Heart rate - Blood pressure - Resp rate - Partial pressure of O2 - Chest x-rays - Fluid balance - Weight loss (1kg/day) - Hourly urine output
62
How does a LBBB appear on an ECG?*
Slide 22 | - Biventricular pacemaker if weak heart to allow coordination
63
Why would you do a full blood count on a patient with heart failure?
- Patients with HF often anaemic | - Anaemia might explain symptoms
64
Why would you do a NTpro-BNP?
- Natriuretic peptide: released in response to ventricular stretch due to fluid overload - Afib can triple
65
Why would you do U&E tests?
- Check for renal function deterioration | - Na/K levels for medication
66
Why would you do LFTs?
Patients' livers can get congested
67
Why would you do clotting tests?
May consider anticoagulants for Afib
68
Why would you check the CRP?
To look for inflammation and infection as a cause
69
What is the NTpro-BNP test?***
- Test for a hormone released in response to atrial and ventricular stretching due to fluid overload - Can triple in Afib - Negative predictive value 97%
70
What does it mean when a patient has a very HIGH BNP?
- Severe heart failure - Heart is working to counteract (natriuresis, diuresis, vasodilation) - Values around 2000 = strong indication of heart failure - Values under 400 = probably not heart failure
71
What is the role of the sympathetic nervous system in the heart?
A baroreceptor-mediated response that aims to improve CO by promoting cardiac contractility, vasoconstriction, tachycardia
72
What is a transthoracic echocardiogram used for?
To check for severe LV impairment
73
What are the long term effects of sympathetic activation?
- Downregulation of beta adrenergic receptors | - Noradrenaline inducing hypertrophy and upregulates RAAS
74
What are the physiological effects of beta-blockers?
1. Reducing heart rate 2. Reducing BP 3. Reduced CO so less oxygen demand
75
How do you prescribe beta-blockers?
- Initiate at a low dose and titrate slowly | - Alter other medication if needed
76
How do you prevent the activation of RAAS in heart failure?
- ARB/angiotensin receptor blockers | - ACE inhibitors
77
What is the function of spironolactone?*
Prevents the aldosterone concentration from rising to prevent arrhythmias
78
How do you manage and treat a patient with HFrEF?***
NYHA I: treat underlying risk factors NYHA II: refer for cardiac rehab, ACEI, ARB, beta blockers, diuretics NYHA III: consider implantable monitoring device, evaluate risk NYHA IV: end of life discussion, ventricular assist device CONSIDER TRANSPLANT AND PALLIATIVE CARE THROUGHOUT THE TREATMENT
79
When is a biventricular pacemaker good?
In heart failure with a NATURAL LOSS OF SYNCHRONY
80
How to approach HFrEF patient with involvement?
- Educate patient - Involve MDT - Cardiac rehabilitation